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Molecular determinants and regulation of Leishmania virulence.

Chang KP, McGwire BS - Kinetoplastid Biol Dis (2002)

Bottom Line: The outcome of each phase is depicted to result from the interactions of a distinct group of parasite molecules with a specific host immune compartment.Their interactions with the host immune system lead to the elimination or reduction of parasites to effect a clinical cure.The model suggests that different parasite determinants may be targeted by different strategies to achieve more effective control of leishmaniasis and other similar diseases.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Microbiology/Immunology, University of Health Sciences/Chicago Medical School, North Chicago, IL, USA. changk@finchcms.edu

ABSTRACT
A Leishmania model to explain microbial virulence in chronic infectious diseases is proposed. All these diseases progress from infection to symptomatic phase to host death or recovery. The outcome of each phase is depicted to result from the interactions of a distinct group of parasite molecules with a specific host immune compartment. The first group consists of invasive/evasive determinants, which are largely parasite cell surface and secreted molecules. Their activities help parasites establish infection by overcoming host immunologic and non-immunologic barriers. These determinants do not cause disease per se, but are indispensable for infection necessary for the development of a disease-state. The second group of parasite molecules consists of "pathoantigenic" determinants - unique parasite epitopes present often within otherwise highly conserved cytoplasmic molecules. Immune response against these determinants is thought to result in immunopathology manifested as clinical signs or symptoms, namely the virulent phenotype. The third group of parasite molecules is hypothetically perceived as vaccine determinants. Their interactions with the host immune system lead to the elimination or reduction of parasites to effect a clinical cure. Differential expression of these determinants alone by parasites may alter their interactions with the hosts. Virulent phenotype is consequently presented as a spectrum of manifestations from asymptomatic infection to fatality. A secondary level of regulation lies in host genetic and environmental factors. The model suggests that different parasite determinants may be targeted by different strategies to achieve more effective control of leishmaniasis and other similar diseases.

No MeSH data available.


Related in: MedlinePlus

Some Leishmania pathoantigenic determinants proposed to cause immunopathology manifested as the clinical symptoms in leishmaniasis. The molecules listed have been found to contain immunogenic B-cell epitopes.
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Figure 2: Some Leishmania pathoantigenic determinants proposed to cause immunopathology manifested as the clinical symptoms in leishmaniasis. The molecules listed have been found to contain immunogenic B-cell epitopes.

Mentions: Fig. 2 lists a number of Leishmania antigens found to elicit antibodies often at high titers in kala-azar patients [10]. The data presented were summarized from articles published by others and some are proposed hypothetically. These Leishmania antigens are identified by Western blot analysis and/or by immunoscreening of Leishmania expression libraries with patients' sera.


Molecular determinants and regulation of Leishmania virulence.

Chang KP, McGwire BS - Kinetoplastid Biol Dis (2002)

Some Leishmania pathoantigenic determinants proposed to cause immunopathology manifested as the clinical symptoms in leishmaniasis. The molecules listed have been found to contain immunogenic B-cell epitopes.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC119322&req=5

Figure 2: Some Leishmania pathoantigenic determinants proposed to cause immunopathology manifested as the clinical symptoms in leishmaniasis. The molecules listed have been found to contain immunogenic B-cell epitopes.
Mentions: Fig. 2 lists a number of Leishmania antigens found to elicit antibodies often at high titers in kala-azar patients [10]. The data presented were summarized from articles published by others and some are proposed hypothetically. These Leishmania antigens are identified by Western blot analysis and/or by immunoscreening of Leishmania expression libraries with patients' sera.

Bottom Line: The outcome of each phase is depicted to result from the interactions of a distinct group of parasite molecules with a specific host immune compartment.Their interactions with the host immune system lead to the elimination or reduction of parasites to effect a clinical cure.The model suggests that different parasite determinants may be targeted by different strategies to achieve more effective control of leishmaniasis and other similar diseases.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Microbiology/Immunology, University of Health Sciences/Chicago Medical School, North Chicago, IL, USA. changk@finchcms.edu

ABSTRACT
A Leishmania model to explain microbial virulence in chronic infectious diseases is proposed. All these diseases progress from infection to symptomatic phase to host death or recovery. The outcome of each phase is depicted to result from the interactions of a distinct group of parasite molecules with a specific host immune compartment. The first group consists of invasive/evasive determinants, which are largely parasite cell surface and secreted molecules. Their activities help parasites establish infection by overcoming host immunologic and non-immunologic barriers. These determinants do not cause disease per se, but are indispensable for infection necessary for the development of a disease-state. The second group of parasite molecules consists of "pathoantigenic" determinants - unique parasite epitopes present often within otherwise highly conserved cytoplasmic molecules. Immune response against these determinants is thought to result in immunopathology manifested as clinical signs or symptoms, namely the virulent phenotype. The third group of parasite molecules is hypothetically perceived as vaccine determinants. Their interactions with the host immune system lead to the elimination or reduction of parasites to effect a clinical cure. Differential expression of these determinants alone by parasites may alter their interactions with the hosts. Virulent phenotype is consequently presented as a spectrum of manifestations from asymptomatic infection to fatality. A secondary level of regulation lies in host genetic and environmental factors. The model suggests that different parasite determinants may be targeted by different strategies to achieve more effective control of leishmaniasis and other similar diseases.

No MeSH data available.


Related in: MedlinePlus